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The consequences of a high-calorie diet background before calorie restriction on skeletal muscles in a mouse model.

ABSTRACT: The beneficial effects of calorie restriction (CR) are numerous. However, there is no scientific evidence about how a high-calorie diet (HCD) background influences the mechanisms underlying CR on skeletal muscles in an experimental mouse model. Herein we present empirical evidence showing significant interactions between HCD (4 months) and CR (3 months). Pectoralis major and quadriceps femoris vastus medialis, in the experimental and control groups, displayed metabolic and physiologic heterogeneity and remarkable plasticity, according to the dietary interventions. HCD-CR not only altered genetic activation patterns of satellite SC markers but also boosted the expression of myogenic regulatory factors and key activators of mitochondrial biogenesis, which in turn were also associated with metabolic fiber transition. Our data prompt us to theorize that the effects of CR may vary according to the physiologic, metabolic, and genetic peculiarities of the skeletal muscle described here and that INTM/IM lipid infiltration and tissue-specific fuel-energy status (demand/supply) both hold dependent-interacting roles with other key anti-aging mechanisms triggered by CR. Systematic integration of an HCD with CR appears to bring potential benefits for skeletal muscle function and energy metabolism. However, at this stage of our research, an optimal balance between the two dietary conditions, where anti-aging effects can be accomplished, is under intensive investigation in combination with other tissues and organs at different levels of organization within the organ system.

SUBMITTER: Maldonado M

PROVIDER: S-EPMC8266348 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionNeuroblastoma is a malignant pediatric cancer derived from neural crest cells. It is characterized by a generalized reduction of mitochondrial oxidative phosphorylation. The goal of the present study was to investigate the effects of calorie restriction and ketogenic diet on neuroblastoma tumor growth and monitor potential adaptive mechanisms of the cancer's oxidative phosphorylation system.MethodsXenografts were established in CD-1 nude mice by subcutaneous injection of two neuroblastoma cell lines having distinct genetic characteristics and therapeutic sensitivity [SH-SY5Y and SK-N-BE(2)]. Mice were randomized to four treatment groups receiving standard diet, calorie-restricted standard diet, long chain fatty acid based ketogenic diet or calorie-restricted ketogenic diet. Tumor growth, survival, metabolic parameters and weight of the mice were monitored. Cancer tissue was evaluated for diet-induced changes of proliferation indices and multiple oxidative phosphorylation system parameters (respiratory chain enzyme activities, western blot analysis, immunohistochemistry and mitochondrial DNA content).ResultsKetogenic diet and/or calorie restriction significantly reduced tumor growth and prolonged survival in the xenograft model. Neuroblastoma growth reduction correlated with decreased blood glucose concentrations and was characterized by a significant decrease in Ki-67 and phospho-histone H3 levels in the diet groups with low tumor growth. As in human tumor tissue, neuroblastoma xenografts showed distinctly low mitochondrial complex II activity in combination with a generalized low level of mitochondrial oxidative phosphorylation, validating the tumor model. Neuroblastoma showed no ability to adapt its mitochondrial oxidative phosphorylation activity to the change in nutrient supply induced by dietary intervention.ConclusionsOur data suggest that targeting the metabolic characteristics of neuroblastoma could open a new front in supporting standard therapy regimens. Therefore, we propose that a ketogenic diet and/or calorie restriction should be further evaluated as a possible adjuvant therapy for patients undergoing treatment for neuroblastoma.

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The consequences of a high-calorie diet background before calorie restriction on skeletal muscles in a mouse model.

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